- Email: [email protected]
Latex allergies in the health care worker
CONTINUING EDUCATION
Latex Allergies in the Health Care Worker Caroline C. Tesiorowski, RN
A dramatic increase in the incidence of latex allergies in health care workers followed the surge in latex glove use accompanying the rise of human immunodeficiency virus (HIV) in the early 1980s. This increase in latex glove use was driven by the release of Universal Precautions issued by the Centers for Disease Control (CDC) in response to the rise of HIV and other blood-borne pathogens. Efforts to stem allergic responses in the workplace have relied on the substitution of other materials for latex. Unfortunately, there is so much latex in everyday life that avoiding this allergen is exceedingly difficult once one is sensitized. Additionally, there are numerous cross reactants that are present in the environment. The situation is further confounded by the introduction of genetically manipulated foods and agricultural products that contain defense proteins genetically inserted to protect plants from pests and pathogens. Many of these defense proteins are antigens that will cross react with latex. Sensitivity reactions, once developed, may progress to the point at which the health care worker is excluded from working. This report provides an overview of rubber products and cross reactants, allergic reactions, and latex sensitivity for the health care worker. © 2003 by American Society of PeriAnesthesia Nurses.
Objectives—Based on the content of this article, the reader should be able to (1) identify at least 3 plant species that produce natural rubber; (2) describe the relationship between the latex glove manufacturing process and latex sensitivity; (3) define the 4 types of allergic reactions; and (4) describe the diagnosis of latex allergy. SINCE 1987, THE number of workers’ compensation claims regarding latex sensitivity have increased significantly in the health care field. These claims involve workers in all health care
Caroline C. Tesiorowski, RN, is a nurse in the PACU at Santa Barbara Cottage Hospital, Santa Barbara, CA. Address correspondence to Caroline C. Tesiorowski, RN, 14 Calle Capistrano, Santa Barbara, CA 93105; e-mail address: [email protected]. © 2003 by American Society of PeriAnesthesia Nurses. 1089-9472/03/1801-0004$35.00/0 doi:10.1053/jpan.2003.50003 18
settings and specialties, including perianesthesia nurses.1 This increase in latex hypersensitivity was triggered by the advent of universal precautions after the rise in acquired immunodeficiency syndrome (AIDS), hepatitis C, and other blood-borne pathogens.2,3 This hypersensitivity, particularly in the health care worker, now raises an emergency public health issue. Margaret Veach, writing in the American Medical News, indicated that estimates of latex medical glove use had jumped from 12 billion pairs in 1987, to more than 200 billion pairs a decade Journal of PeriAnesthesia Nursing, Vol 18, No 1 (February), 2003: pp 18-31
LATEX ALLERGIES IN THE HEALTH CARE WORKER
later. Because the demand sometimes exceeded supply, some manufacturers were prone to cut corners on the processing necessary to remove allergens. Others, in their rush to the market, used less-expensive processes that actually increased these adverse characteristics.4
Significance of Latex Allergy in the Health Care Worker Latex allergies currently affect an estimated 10% to 12% of health care workers3,5 and up to 24% of anesthesiologists.5 It is estimated that 10% of these people are immunoglobulin E (IgE) positive and in the early stages of sensitization, but clinically asymptomatic.5 Others, however, estimate that the figure for those sensitized but not clinically having reactions may be as high as 50%.6 Based on the most conservative of these estimates, it is possible that an average of 2 to 5 PACU nurses of every 20 may already be sensitized.
19
erative setting, staff may still be continuously exposed in other areas of the hospital because airborne particulate matter remains an unresolved issue. The amount of particulate does not have to be extreme. Baur et al13 noted that the probable threshold for latex aeroallergens is 0.6 ng/m3 for health care workers who have been previously sensitized. Charous et al14 noted that even while using personal latex precautions, a dental assistant with latex allergy and occupational asthma was still exposed to latex aeroallergens in the workplace because of latex that had settled into or was part of clinic upholstery fabric, as well as carpet dust. Thus, merely controlling for latex in the particular workstation or job may be insufficient. Additionally, numerous and ubiquitous crossreacting allergens exist in most metropolitan and urban environments. Thus, even after removing oneself from the health care workplace, the highly sensitized individual may still be continuously exposed in an office situation in which this form of air pollution is a factor. For example, tire dust, an ubiquitous air pollutant in any metropolitan center, is an agonist allergen and cross reacts in natural rubber latex (NRL) allergy.15-19 It has also been found that birch pollen and certain other cereal-derived ␣-amylases exacerbate or cross react with rubber product materials.
Brown et al7 noted that latex sensitivity groups were twice as likely to be associated with an inherited or familial heightened sensitivity to allergens (atopy) as compared with nonsensitized groups. Atopy is characterized by a history of asthma, eczema, and allergic rhinitis. Studies show that on average, the first clinical symptoms appeared after 5 years of exposure in those using latex gloves in the workplace.8,9 This seems reasonable because about 6 years elapsed between the Centers for Disease Control’s (CDC) replacement of the “Blood and Body Fluids Precautions” with Universal Precautions in 1983, and the first major reports of latex reactions in 1989. Certain patient populations may offer a glimpse of the potential for developing hypersensitivity by repeated exposure. The theory of hypersensitivity by repeated exposure is further confirmed by the high percentage of reactivity (60% to 70%) found in children with spina bifida.10-12
The use of rubber in products is ubiquitous throughout society because the world’s natural rubber use currently approximates 4,500,000 tons annually.20 An understanding of rubber products and their cross reactants is crucial in the diagnosis and management of latex hypersensitivity.
Although some controls can be applied to limit exposure to latex allergens for sensitized patients and staff in the perianesthesia and periop-
Natural rubber latex is one of several products made from rubber. The term latex originally applied only to the sap of rubber-producing
Rubber Products and Cross Reactants
CAROLINE C. TESIOROWSKI
20
plants. With common use, however, the term has come to represent both the uncured natural and the synthetic rubber products. The term rubber is thought to come from an early serendipitous use in which a wad of the raw sap coagulant was found to rub off pencil marks in the British record books on rubber plantations. We now call this an eraser. The commercial applications of NRL include dipped goods such as gloves and condoms, as well as adhesives in pressure-sensitive tape. Approximately 40,000 household and medical products contain latex, making it difficult, if not impossible, to avoid contact with latex allergens.21-23 Although most natural rubber latex is obtained commercially from the Hevea braziliensis rubber tree, there are about 200 plant species that produce natural rubber. These include common dandelion, goldenrod, and members of the sunflower family. Sunflower has been shown to contain serious contact allergen contents. Nonetheless, there are several common members of this family that include many edible salad plants such as lettuce, endive, chicory, and artichoke. Other members of this family include chrysanthemums, as well as many common weeds and wildflowers. Also included are cultivated species such as marigolds, daisies, and sunflowers, the oils and seeds of which are found in many baked products.19 Unfortunately, species within the sunflower group will cross react with the plants within the Umbelliferae family, named for the umbrellashaped flowering stand.19 There are a surprisingly large number of plants in this family that are used as foods or spices. Examples include carrots, parsley, celery, and fennel. Additionally, there are discussions about nickel cross reacting with these plant materials.24 The principal protein molecule of rubber is 1-4 cis-polyisoprene (1-4 CP). This molecule, in common with natural rubber, is also found in many plant species. Data indicate that more
than 2,000 plant species contain 1-4 CP. This family of isoprenoids comprises more than 200,000 different molecules that are found in cell membranes and cellular structures of both plants and animals. Isoprenoids also act as electron carriers and are important in cellular energy. Numerous isoprenes are also involved in defense proteins built by plants against pests and pathogens.25,26 Rubber in its natural state generally is not considered an allergen.26 Nonetheless, in harvesting rubber, the trees are scribed to create wounds that drip sap. In response to this repeated wounding, the tree produces defense proteins that are incorporated into the sap that eventually becomes the latex product. Natural latex is comprised of somewhat more than 250 polypeptides, of which 60 have IgE-binding tendencies that may result in allergic reactivity.27 These polypeptides are chains of amino acids, and each protein is made up of one or more polypeptide chains. Several rubber proteins or their polypeptide fragments have been linked to allergies. Reaction to the 4.7-kDa polypeptide, Hevein, has been detected in enzyme-linked tests in 75% of the sera from health care workers allergic to latex. Positive skin test results to this polypeptide were also noted in 81% of patients with latex allergies.27-29 The 14-kDa rubber elongation factor (Hev b 1) is also a major player in the allergy.30 Other proteins identified as latex allergens include the following:
● ● ● ●
Hevein C domain, 14 kDa Prohevein, 20 kDa Profilin, 14 to 15 kDa Hevamin and other 29- to 33-kDa proteins ● 45-kDa protein ● 27-kDa in patients with spina bifida These proteins are absorbed in glove powder, which is an allergen carrier. In some gloves, these proteins leach out and become available to the skin.31,32
LATEX ALLERGIES IN THE HEALTH CARE WORKER
Rubber Processing Rubber processing is a vast complexity of chemical reactions. It requires the blending, at various critical stages, of a large host of chemical additives. These additives are used to give strength, elasticity, longevity, color, texture, and a myriad of other properties to rubber. Such chemicals also include flame retardants, fungicides, ultraviolet absorbers and blocking agents, stabilizers, and dozens of antioxidants to reduce deterioration.33-35 During the processing of sap from the rubber plant, ammonia is used to prevent coagulation and also to extend storage. Further processing, however, necessitates deammoniation, which requires formaldehyde. Formaldehyde was shown to sensitize up to 24% of patients in one study.33 In addition, there is also evidence of mutagenicity, as well as cases of lymphomas caused by formaldehyde.34,35 For these reasons, low ammonia sap processing is preferred. This technique, however, requires different chemicals for stabilization and preservatives. These chemicals may leach from the finished product, causing serious toxic effects. Chemicals associated with the more serious toxic effects are tetramethylthiram disulfide (examples of this chemical family include Antabuse and some commercial agricultural fungicides) and dithiocarbamate (related to the “nerve gas” cholinesterase-inhibiting pesticides). The thirams are in fact derivatives of dithiocarbamates. The combined alcohol-thiram (Antabuse) reaction is not an allergic response, but rather a toxic response accruing to enzyme blockage. When aldehyde dehydrogenase is blocked, this allows for the accumulation of toxic levels of acetaldehyde. Thus, topical exposure through latex gloves to thiram is sufficient to initiate an “Antabuse reaction” and can affect the innocent social drinker. The reaction can also exacerbate lesions of allergic contact dermatitis.26 Latex gloves are relatively easy to manufacture. Because of the high demand for cheap latex
21
gloves, many small and inexperienced foreign firms went into business during the initial peak demand of the mid to late 1980s. These firms attempted to produce high volumes with rushed production, leading to 2 significant results. The necessary wash and rinse cycle for the finished gloves was greatly reduced. More importantly, however, there was a tendency to overdose the latex with accelerators, activators, and sulfur to quicken the reaction time and machine speed. Unfortunately, this excessive use of additives and compounding ingredients exceeded the solubility in the rubber, allowing leaching, which then brought these additives as well as the reacting proteins into direct contact with the user and the patient. This extractable latex allergen level in latex gloves may vary more than 500-fold in different brands.36,37 These added chemicals can be highly toxic and are a main source of sensitizers. Additionally, rubber products may be admixtures of natural and synthetic rubbers. The distinction between rubber and plastic can also be spurious because both contain the same antioxidants, stabilizers, and catalysts.26 About one third of the chemicals used in rubber processing are also used in plastics.38 A classic example of the junction between rubber and plastic is polyurethane. This plastic is known to induce tissue reactions that produce very thick wound capsules around implanted devices.39
Cross Reactants When the immune system mistakenly identifies a similarly shaped protein molecule or chemical composition for an allergen, adverse reactions occur. This is known as cross reactivity. Such cross reactivity is caused by a wide number of structurally related proteins that plants can potentially produce, and that are mimicked in the cellular machinery of humans. Many of these defense proteins arise from ancient ancestral organisms that have common lineages with both plants and animals. Nature has thus produced highly conserved evolutionary processes for defense that worked for most of life’s evo-
CAROLINE C. TESIOROWSKI
22
lution and development, but now conflict with modern chemistry and genetically engineered foods and fibers.19 There are a wide number of natural and manmade environmental cross reactants that exacerbate latex sensitivity. Defense proteins are genetically engineered proteins for insertion into plant genes to improve their resistance to pests and diseases. More and more genetically modified foods are being produced that contain these defense proteins. Unfortunately, these products constitute major cross-reacting allergens with NRL. IgE-bound reactions occur with “prohevein,” which is one of the major allergens in NRL, and also to other proheveinlike defense proteins in 70% to 88% of persons allergic to NRL.40 Prohevein-like defense proteins are also found in tobacco.41 Thus, once sensitized to NRL, smokers and those exposed to “second-hand” smoke may see their health increasingly affected.
Allergic Reactions Allergic reactions are the most common form of immunologic response and involve the T and B cells in an antibody-immunoglobulin–mediated response to foreign antigens (allergens). The result can range from local tissue inflammation to systemic organ dysfunction. Of the 5 immunoglobulins present in the body, 3 are involved in allergic hypersensitivity reactions. These immunoglobulins are IgG, IgM, and IgE. The reactions stimulated by these immunoglobulins are classified into 4 distinct types (types I through IV). Type I Reaction
A type I reaction is an IgE-mediated hypersensitivity involving antibodies on the mast cells. Reaction with an allergen causes the mast cell to degranulate and release vasoactive and inflammatory mediators. The reaction occurs within minutes, and the result may be seen locally in such responses as allergic rhinitis, angioedema, or atopic dermatitis. Atopic individuals are more prone to experiencing this
reaction. Anaphylaxis is also a type I reaction. The antibody response in anaphylaxis is a generalized, whole-body response. Type II and III Reactions
Type II and III reactions involve both IgG and IgM. These types of reactions generally are not involved with latex. A type II reaction is seen in complement reactions associated with cellbound reactions and generally is not associated with allergens. Type III reactions are an immune complex hypersensitivity associated with an allergen that activates the complement cascade. With high concentrations of both allergen and antibody, an Arthus reaction may occur. This reaction generally results from an injection and is seen as a localized skin inflammation, at times with hemorrhage, and occasionally followed by necrosis and ulceration. In contrast to the more immediate type I reaction, a type III reaction develops over 4 to 10 hours.42-44 Type IV Reaction
Type IV reactions are delayed-type reactions mediated by helper T lymphocytes. These reactions are commonly seen in contact dermatitis with latent developing symptoms. Latex allergens may also be involved. Symptoms may begin to appear within 24 hours of exposure, but there can be a lag of several days. Poison oak would be an example of a type IV reaction. Another example of this reaction is the tuberculin reaction.44,45
Latex Reactions Latex reactions fall into either the type I (immediate type reaction) or type IV (delayed reaction) categories. Reactions noted may include vertigo, urticaria, contact dermatitis, naso-rhinitis, upper respiratory tract irritation, conjunctivitis, local angioedema, asthma, hypotension, and anaphylactic shock, which can end in death. Type I Allergic Reaction: The Immediate Reaction
Onset of symptoms for type I, the immediate reaction, may be seen as early as a few minutes
LATEX ALLERGIES IN THE HEALTH CARE WORKER
after exposure. For example, anaphylaxis in the operating theater usually starts within 30 minutes after the procedure is started. This rapid response is not necessarily the rule, however. A reaction involving complete collapse may also occur a few hours after exposure. Thus, the exposed nurse may finish the shift and be on a congested freeway when hit with anaphylaxis. Type I reactions to latex can include a wide range of signs and symptoms as shown in Table 1.44-46 Type IV Allergic Reaction: The Delayed Reaction
A type IV reaction is a delayed reaction that may occur hours after the exposure to the allergen. Type IV reactions often present as secondary lesions from contact dermatitis and arise from a loss of barrier function in the irritated skin and tissue. Dermatitis related to latex gloves is seen in 2 different forms; however, only one is an allergic response. The most common response is irritant contact dermatitis, which is a nonallergic response making up 75% of cases.43 Signs and symptoms are dry, itchy, irritated areas on the skin of the hands. Marked erythema is sharply demarcated, and this may be associated with numerous vesicles.42-44 Dermatitis distribution is the single most important clue in distinguishing the 2 reactions. With irritant contact dermatitis, the skin above the glove line is usually spared as the skin reaction arises from the irritation of the gloves and added powders.42,44 Allergic contact dermatitis is a type IV, T cell– mediated response comprising 25% of cases. Symptoms may appear in 24 hours and crest in about 48 hours. Each exposure builds greater sensitivity.43 This reaction results from the chemicals added to latex during harvesting, processing, or manufacturing. The pathophysiology requires a prior sensitizing contact to a specific allergen. There may be repeated contacts and no apparent reaction. The reaction to the allergen usually occurs at the site of contact anywhere from 5 to 7 days, and occasionally as long as 20 days after the initial or sensitizing
23
Table 1. Signs and Symptoms of Latex Allergy: Type I, the Immediate Reaction Atopic Allergic rhinitis, nasal and conjunctival discharge accompanied by pruritis, erythema, and excessive tearing Allergic asthma, hayfever, bronchial asthma accompanied by wheezing and tightness of the chest, dyspnea, and cough Allergic dermatitis, pruritis, hives accompanied by erythema with edema and pruritis, followed by vesicles and bullae. Later the skin weeps, followed by crusting and secondary infection Allergic gastroenteropathy from ingested allergens may be accompanied by skin reactions such as urticaria and angioedema. Anaphylactic Initial symptoms Tingling lips and mouth Flushing of face, body Itchy eyes, nose, face Eyes and face swelling Nausea Hives Wheezing Hoarseness Respiratory symptoms Dyspnea Retrosternal pain Stridor Tachypnea Wheezing Cardiovascular symptoms Palpitations Tachycardia Arrhythmias Hypotension Syncope Arrest Cutaneous symptoms Pruritis Edema Erythema Hives Gastrointestinal symptoms Nausea Vomiting Abdominal cramps Diarrhea Advancing symptoms of anaphylaxis Anxiety and feeling of doom Weakness and dizziness Laryngeal edema Laryngeal obstruction Inability to breath Shock Loss of consciousness Arrest Data from Calfran et al,44 Tierney et al,45 and AORN.46
24
contact. The site, once reacting, is characterized by a perivascular accumulation of mononuclear cells causing leaking of endothelial cells and microvascular permeability.44 There are no circulatory or otherwise detectable antibodies produced, although there is a local tissue allergy.43 On staining with immunoperoxidase, there is a predominance of CD4 T lymphocytes in the perivascular tissue. These lymphocytes then differentiate into T1 cells that secrete cytokines, the responsible mechanism for the delayed reaction.44 Symptoms may then develop in 24 to 48 hours after the second exposure to the allergen (6 hours to 7 days). The first symptoms, however, can develop after years of continued exposure. With removal of the offending allergen, the reaction will generally resolve after 2 to 3 weeks. Unfortunately, this condition is usually, though not invariably, lifelong. Thus, later recontact after a long period of isolation from the offending allergen may instigate the reappearance of the problem.42-44 Because rubber products are ubiquitous, there may be continued non-workplace exposures. In allergic eczematous contact dermatitis, the acute lesions may be red, swollen, and weeping. Crusting lesions may appear after a few days. In chronic cases, skin scaling and fissuring are dominant.42-44 In addition to latex gloves used at the work site, causes may include fabric finishes, dyes, oils, tars, rubber, soap, cosmetics and perfume, insecticides, wood resins, plants, paints, plastics, glues, fiberglass, metals, polishes, and ointments.43 This contact dermatitis may also be associated with medications. The main pharmacotherapeutic agents involved are rheumatologic agents, including NSAIDs. Dermatologic, ophthalmologic, pneumologic, and cardiovascular drugs are also implicated. These medications can include the caine anesthetics; antihistamines such as pyribenzamine; or antibiotics such as neomycin, furacin, penicillin, or sulfa. Because people often unconsciously rub their eyes, the eyelids also can be the site of intense edema and vesiculation with erythema.42-44 Type IV glove dermatitis can be reduced by switching to eudermic products. Health care
CAROLINE C. TESIOROWSKI
workers with type IV allergic responses can obtain the required level of job-related protection from nitrile, vinyl, or other synthetic gloves. When latex gloves are required, powder-free gloves with reduced protein content should be used. The term hypoallergenic does not necessarily mean that the gloves contain lower protein allergen content. Consequently, the designation as hypoallergenic should not be the main criterion in determining alternatives.47
Latex Allergy and the Health Care Worker Most forms of type I allergy caused by environmental allergens other than latex can be treated by pharmacotherapy or specific immunotherapy. The health care industry has adopted a policy of minimizing exposure to latex proteins through the provision of other materials. Originally, this was thought to represent a costeffective, preventative measure for latex allergy, especially in the hospital setting. Recent available studies, however, now seem to raise some questions as to whether simply replacing latex with nonallergenic materials is sufficient. Williams and Halsey48 showed the existence of extremely small respirable particulate matter associated with either the powder or a bacterial contaminate formed during the production of latex gloves. These small particles carry the latex allergen into the air and remain airborne for hours. Once airborne, these particles become part of the internal hospital air supply. The hospital’s large ventilation systems then assure that the particles are broadly distributed and recirculated.49 The last 2 decades have seen a rise in type I reactions from latex products. Initial reactions may start with relatively vague symptoms that include a suddenly stuffy nose, oropharyngeal swelling, and difficulty swallowing. This may be followed by anxiety, dyspnea, tachypnea, retrosternal pain and tightness of the chest, perspiration, and pallor. From there, full shock can develop. This reaction is now recognized as a rapidly growing clinical crisis.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
It is not merely the wearing of latex gloves that can affect the previously sensitized health care worker. The worker may be exposed in many ways that she/he would not suspect because these exposures are not limited to the work environment and may involve the health care worker as a patient. Tan et al50 and others51,52 discuss the perioperative collapse of patients who were previously sensitized to latex and cross reacted with certain anesthetic agents. Additionally, some cross sensitivity may occur with the use of alcohol to clean skin surfaces because alcohol and alcohol-containing lotions may react with thiram, a chemical used in the processing of latex. This reaction can lead to either continued skin sensitivity or an Antabuse reaction. Cross-reacting ingredients must also be considered in the planning and preparation of hospital meals because cases of anaphylactic reactions in hospital patients arising from cross reactivity with food items have been noted.53,54 Health care workers employed in large publicly funded health care systems may also be at increased risk as these and other systems often depend on the typical “least-cost” contractor for supplied items. Williams and Halsey48 showed that gram-negative bacterial endotoxins (GNBE) are a highly significant contaminant of some glove manufacturing processes. The effects of GNBE include skin irritation and the potential for accompanying secondary lesions, induced respiratory problems, fever, and shock. The highest levels of endotoxin were found in nonsterile examination gloves, an item that is often purchased on a “least-cost” contract. Although there was a greater tendency for powdered gloves to contain more endotoxins and reactive
25
proteins, this problem was also noted in nonpowdered gloves in which these highly respirable GNBE particles were mainly found on the inside of the gloves. These particles are not physically associated with the powder and are easily released into the air on the “explosive” snap as the gloves are pulled off. GNBE may be responsible for the disproportionate enhancement of delayed and immediate hypersensitivity reactions to the chemicals and proteins found in latex gloves. This problem may be exacerbated by sterilization, as Shmunes and Darby55 reported that sterilization of similar gloves by gamma irradiation actually increased the endotoxin levels. Further, it was found that the use of ethylene oxide caused a reaction with the rubber accelerators in gloves. The new products produced by this reaction were capable of causing irritant dermatitis and chemical burn. These effects did not dissipate with the gas but remained active for months in wrapped and stored materials.56-61 An initial development of hypersensivity to latex may affect not only one’s employment, but everyday activity as well. Numerous allergens of latex are also found to cross react with a broad variety of environmental allergens,62-64 thus raising the potential for hypersensitivity reactions outside of the work environment as well. Materials known to cross react with and exacerbate latex hypersensitivity are noted in Table 2.
Diagnosis of Latex Allergy Latex allergy should be ruled out for anyone developing the following symptoms after latex exposure: irritated red hands; irritation involving nasal passages, sinuses, eyes, shortness of
Table 2. A List of Common Latex Cross Reactants Fruits and nuts Apple, apricot, avocado, banana, cherry, chestnut, coconut, fig, kiwi fruit, loquat, mango, melons, papaya, passion fruit, peach, strawberries, sunflower seed, watermelon Vegetables Buckwheat, carrot, fresh yellow pepper, other peppers, potato, tomato, turnip Animal products Crustacea, fish, shellfish, snails Other allergens Auto tire dust, bacterial endotoxins, birch and cedar pollens, certain anesthetic agents, sunflower family, tobacco, Ficus benjamina
CAROLINE C. TESIOROWSKI
26
breath, coughing, or wheezing; hives; or unexplained shock. Health care workers experiencing these symptoms should be appropriately evaluated because once sensitized, continued exposure may end in a serious allergic reaction. Diagnosis entails a thorough medical history, physical examination, and laboratory tests. Food and Drug Administration (FDA)–approved blood tests are now available for detecting latex antibodies. Additionally, there are standardized protocols for skin tests; however, no standardized latex extract is currently available. Skin testing extracts to determine latex protein allergy include commercial extracts, latex glove extracts, and extracts of hevea leaves. Testing has to be performed with the allergen against which the patient is presumed to be allergic. The different types of available allergen extracts, however, may not contain the particular allergen. One extract used in Canada (Bencard Laboratories, Mississauga, Ontario) has been reported to have 93% sensitivity to latex.65 Glove extracts are made using a standardized method of soaking glove material in diluent. Extreme caution must be used with glove extracts because of variable allergenic protein levels and the potential for serious reactions from skin tests.66,67 Conversely, false-negative skin tests may also be produced by extracts of gloves with low latex allergen content. Skin testing with allergen extracts has traditionally been considered the most sensitive means of detecting IgE antibodies. Although often considered the gold standard, this process is not without risk and therefore should be performed only at medical centers with staff that are experienced and equipped to handle severe reactions. The pinprick introduces latex into the skin and a positive result produces dermal edema and reddening. Certain fruits such as banana, avocado, chestnut, and kiwi fruit (Table 2) may cross react with latex in allergy testing in the atopic individual. If the health care worker is also exposed to glutaraldehyde (Cidex, Sporocidin), testing for this should also be included.
Allergens that should be routinely tested include the following68: black rubber mix, 1%; carba mix, 3%; ethylenediamine 2HCL, 1%; imidazolodinyl urea, 2%; mercaptobenzothiazole, 1%; mercapto mix, 1%; O-phenylenediamine, 1%; thiram mix, 1%; triclosan, 2%; volunteersupplied latex glove. In vitro tests are available and are safer because the laboratory can determine the presence of IgE antibodies specific to latex from a drawn blood sample. A number of tests exist in the marketplace that give good results with freedom from the danger of immediate hypersensitivity associated with skin-prick testing.69 For the interested reader, more information may be found on the American Society of Anesthesiology Web page, www.asahq.org/Newsletters/ 1999/05_99/Latex_0599.html.70 Once sensitized to latex, individuals may need to considerably alter their current lifestyle to accommodate the ubiquitous nature of latex and cross reactants. At some point, the hypersensitivity may reach a level at which there is a considerable risk for the development of anaphylactic shock. The individual would then need to carry self-injecting equipment for continued safety. With the added insults to the immune system, there is the added risk of multiple chemical sensitivity syndrome.71-73 This syndrome is controversial but is recognized in worker compensation claims, tort liability, and regulatory actions. Unfortunately, once this level of disability is achieved, little can be done for the lost earning power, and current government support and compensation programs offer a dismal prospect.
Conclusion Latex sensitivities in health care workers continue to rise. Reactions are often dramatic and unpredictable because a mild sensitivity can convert to anaphylactic shock after multiple or continued exposure. An awareness of reaction classifications, exposure routes, and diagnosis techniques is critical in avoiding continued exposure and possible adverse outcomes.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
27
References 1. Gelman JL: United States Workers’ Compensation Programs are Becoming Sensitized to Latex. Update on the Law. . . Latex Allergy Litigation. Volume 21, Issue 7. November 1999. Available at www.gelmans.com/articles/latexsurvey99/ latexsurvey1199l.htm. Accessed December 23, 2002 2. Chardin H, Desvaux FX, Mayer C, et al: Protein and allergen analysis of latex mattresses. Int Arch Allergy Immunol 119:239-246, 1999 3. Mahler V, Fischer S, Fuchs T, et al: Prevention of latex allergy by selection of low-allergen gloves. Clin Exp Allergy 30:509-520, 2000 4. Veach M: Allergies to latex gloves hand health workers a growing concern. Available at www.latexallergylinks.tripod. com. Accessed June 14, 2002 5. Holzman RS, Katz JD: Editorial reviews. Anesthesiology 89:287-289, 1998 6. Kowalczyk L: Allergy hazard: Growing number of health care workers developing dangerous reactions to latex. Patriot Ledger April 1, 1997, pp 1-2 7. Brown RH, Schauble JF, Hamilton RG: Prevelance of latex allergy among anesthesiologists. Anesthesiology 89:292-299, 1998 8. Allmers H, Kirchner B, Huber H, et al: The latency period between exposure and symptoms in allergy to natural latex. Deutche Med Wochen 121:823, 1996 9. Esterhuizen TM, Hnizdo E, Rees D: Occurrence and causes of occupational asthma in South Africa—Results from SORDSA’s Occupational Asthma Registry, 1997-1999. S Afr Med J 91:509-513, 2001 10. Elsworth PL, Merguerian PA, Klein RB, et al: Evaluation and risk factors of latex allergy in spina bifida patients: Is it preventable? J Urol 150:691-693, 2001 11. Konz KR, Gjia JK, Kurup VP, et al: Comparison of latex hypersensivity among patients with urologic defects. J Allergy Clin Immunol 95:950-954, 1995 12. Kattan H, Harfi HA, Tipirneni P: Latex allergy in Saudi children with spina bifida. Allergy 54:70-73, 1999 13. Baur X, Chen Z, Allmers H: Can a threshold limit value for natural rubber latex airborne allergens be defined? J Allergy Clin Immunol 101:24-27, 1998 14. Charous BL, Schuenemann PJ, Swanson MC: Passive dispersion of latex aeroallergen in a health care facility. Ann Allergy Asthma Immunol 85:285-290, 2000 15. Williams PB, Buhr MP, Weber RW, et al: Latex allergen in respirable particulate air pollution. J Allergy Clin Immunol 95:88-95, 1995 16. Williams PB, Akasawa A, Dreskin S, et al: Respirable tire fragments contain specific IgE-binding and bridging latex antigens. Chest 109:13S, 1996 (suppl 3) 17. Pope CA, Thun MJ, Namboodiri MM, et al: Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. Am J Respir Crit Care Med 151:669-674, 1995 18. Miguel AG, Cass GR, Weiss J, et al: Latex allergens in tire dust and airborne particles. Environ Health Perspct 104:11801186, 1996 19. Vallon C, Sainte-Laudy J, Guerin JC: Asthma by proxy (to latex of a condom). General review based on an observation. Allerg Immunol (Paris) 26:248-256, 1994 20. GillenA:Biopolymers—Naturalrubber.Availableatwww. Naturalrubber.cjb.net. Accesses June 14, 2002
21. Redman MC: Latex allergy: Recognition and perioperative management. J Post Anesth Nurse 11:6-9, 1996 22. Goffin V, Kharfi M, Pierard-Franchimont C, et al: Latex allergy—When uncertainty remains the only certainty. Rev Med Liege 56:165-169, 2001 23. Latex allergy alert—Update. Available at www.specialclothes.com/latex.htm. Accessed June 17, 2002 24. Ricciardi L, Gangemi S, Isola S, et al: Nickel allergy, a model of food cellular hypersensitivity? Allergy 56:109-112, 2001 (suppl 67) 25. D’Auzac J: From sucrose to rubber: Hevea as a “green rubber factory.” Physiology of latex production. Available at www.irrdb.org/hevea/auzac. Accessed December 16, 2002 26. Taylor JS: Rubber, in Fisher AA (ed): Fisher’s Contact Dermatitis (ed 3). Philadelphia, PA, Lea & Febiger, 1986 27. Posch A, Chen-Heimsoth M: Latex allergens: A review of current knowledge. Pneumologie 51:1058-1062, 1977 28. Kurup VP, Yeang HY, Sussman GL, et al: Detection of immunoglobulin antibodies in the sera of patients using purified latex allergens. Clin Exp Allergy 30:359-369, 2000 29. Chen Z, Posch A, Lohaus C, et al: Isolation and identification of hevin as a major IgE-binding polypeptide in Hevea latex. J Allergy Clin Immunol 99:402-409, 1997 30. Rauf-Heimsoth M, Chen Z, Rihs HP: Analysis of T-cell reactive regions and HLA-DR4 binding motifs on latex allergen Hev b 1 (rubber elongation factor). Clin Exp Allergy 28:339348, 1998 31. Tomazic VJ, Shampaine EL, Lamanna A, et al: Cornstarch powder on latex products is an allergen carrier. J Allergy Clin Immunol 93:751-758, 1994 32. Lundberg M, Wrangsjo K, Johansson SGO: Latex allergens in glove powdering slurries. Allergy 50:378-380, 1995 33. Epstein E, Maibach HI: Formaldehyde allergy. Arch Dermatol 94:186, 1966 34. Speit G, Merk O: Evaluation of mutagenic effects of formaldehyde in vitro: Detection of crosslinks and mutations in mouse lymphoma cells. Mutagenesis. 17:183-187, 2002 35. Merk O, Speit G: Significance of formaldehyde-induced DNA-protein crosslinks for mutagenesis. Environ Mol Mutagen 32:260-268, 1998 36. Jones R, Scheppmann D, Heilman D, et al: Prospective study of extractable latex allergen contents of disposable medical gloves. Ann Allergy 73:321-325, 1994 37. Yunginger J, Jones R, Fransway A, et al: Extractable latex allergens and proteins in disposable medical gloves and other rubber products. J Allergy Clin Immunol 93:836-842, 1994 38. Blue Book. Materials, compounding ingredients and machinery for rubber. New York, NY, Bill Publishing, 1983 39. Shanklin DR, Smalley DL: Dynamics of wound healing after silicon device implantation. Exp Mol Pathol 67:26-39, 1999 40. Bowles DJ: Defense-related proteins in higher plants. Ann Rev Biochem 59:873-907, 1990 41. Hanninen AR, Kalkkinen N, Mikkola JH, et al: Proheveinlike defense proteins of tobacco is a cross reactive allergen for latex-allergic patients. J Allergy Clin Immunol 106:778-779, 2000 42. Odom WD, James RB, Berger TG (eds): Andrews’ Diseases of the Skin: Clinical Dermatology (ed 9), Philadelphia, PA, Saunders, 2000 43. Sheard C: Contact dermatitis. Internet Dermatology So-
CAROLINE C. TESIOROWSKI
28
ciety, Stamford, Connecticut. Last update February 2, 1997. Available at www.lemedicine.org/contact.htm. Accessed June 17, 2002 44. Coltran RS, Kumar V, Collins T (eds): Robbins Pathologic Basis of Disease (ed 6). London, England, Saunders, 1999, pp 195-206 45. Tierney LM, McPhee SJ, Papadakis MA (eds): CMDT (ed 3). Norwalk, CT, Appelton & Lang, 1994, pp 655-657 46. AORN: AORN latex guideline from Standards, Recommended Practices and Guidelines 1999. Denver, CO, Assn of Operating Room Nurses Inc, 1999, p 107 47. A Hazard Alert From the Department of Labor and Industries About Latex Allergy. November 1997. Available at www.lni.wa.gov/wisha/hazalerts/hz972.htm. Accessed December 16, 2002 48. Williams PB, Halsey JF: Endotoxin as a factor in adverse reactions to latex gloves. Ann Allergy Asthma Immunol 79:303310, 1997 49. Charous BL, Schuenemann PJ, Swanson MC: Passive dispersion of latex aeroallergen in a health care facility. Ann Allergy Asthma Immunol 85:285-290, 2000 50. Tan BB, Lear JT, Watts J, et al: Perioperative collapse: Prevalence of latex allergy in patients sensitive to anesthetic agents. Contact Dermatitis 36:47-50, 1977 51. Laxenaire MC, Mertes PM: Anaphylaxis during anaesthesia. Results of a two-year survey in France. Br J Anaesth 87:549-558, 2001 52. Baulig W, Fisy B, Otto G, et al: Latex allergy. Perioperative management in anesthesia and cardiac anesthesia. Anaesthesist 50:861-868, 2001 53. Abeck D, Boerries M, Kuwert C, et al: Anaphylactic reactions to food items with latex allergy. Hautarzt 45:364-367, 1994 54. Ganglberger E, Radauer C, Wagner S, et al: Hev b 8, the Hevea brasiliensis latex profilin, is a cross-reactive allergen of latex, plant foods and pollen. Int Arch Allergy Immunol 125: 216-227, 2001 55. Shmunes E, Darby T: Contact dermatitis due to endotoxin in irradiated latex gloves. Contact Derm 10:240, 1984 56. Taylor JS: Dermatologic hazards from ethylene oxide. Cutis 19:198, 1977 57. Sexton RJ, Henderson EV: Dermatological injuries by ethylene oxide. J Ind Hyg Tox 31:29, 1949 58. Leonard JC, Morin C: Industrial progress concerning
latex allergy in surgery. Rev Chir Orthop Reparatrice Appar Mot 85:727-730, 1999 59. Romaguera C, Vilaplana J: Airborne occupational contact dermatitis from ethylene oxide. Contact Derm 39:85, 1998 60. Tiukhtin VG: Gas chromatographic determination of ethylene oxide residue in sterilized medical items. Gig Sanit Jan-Feb(1) :50-51, 1996 61. Baranova NI, Rudenko BA, Likhtman TV: Gas chromatographic determination of micro-quantities of ethylene oxide in polymeric articles for medical use. Gig Sanit Apr(4) :64-66, 1985 62. Hanninen AR, Mikkola JH, Kalkkinen N, et al: Increased allergen production in turnip (Brassica rapa) by treatments activating defense mechanisms. J Allergy Clin Immunol 104: 194-201, 1999 63. Blanco C, Carillo T, Castillo R, et al: Latex allergy: Clinical features and cross-reactivity with fruits. Annl Allergy 73:309-314, 1994 64. Blanco Guerra C: Latex-fruit syndrome. Allergol Immunopathol (Madr) 30:156-163, 2002 65. Turjanmaa K, Reunala T, Alenius H, et al: Allergens in latex surgical gloves and glove powder. Lancet 336:1588, 1990 66. Yunginger JW: Diagnostic skin testing for natural rubber latex allergy. J Allergy Clin Immunol 102:351-352, 1998 67. Yunginger JW: Latex allergy in the workplace: An overview of where we are. Ann Allergy Asthma Immunol 83:630633, 1999 68. Vyas A, Pickering CA, Oldham LA, et al: Survey of symptoms, respiratory function, and immunology and their relation to glutaraldehyde and other occupational exposures among endoscopy nursing staff. Occup Environ Med 57:752759, 2000 69. Preventing Allergic Reactions to Natural Rubber Latex in the Workplace. Washington, DC, NIOSH, June 1997, DHHS (NIOSH) Publication No. 97-135 70. Thomas LC, Skerman JH: Latex allergy: Another complication for anesthesiology, part 2. Available at www.asahq.org/ Newsletters/1999/05_99/Latex_0599.html. Accessed December 16, 2002 71. Gots RE: Multiple chemical sensitivities—Public policy. [Editorial] J Toxicol Clin Toxicol 33:111-113, 1995 72. American Medical Association Council on Scientific Affairs: Clinical ecology. JAMA 268:3465-3467, 1992 73. Miller CS: Chemical sensitivity: Symptom, syndrome or mechanism for disease? Toxicology 111:69-86, 1996
Latex Allergies in the Health Care Worker 1.2 Contact Hours Directions: The multiple choice examination below is designed to test your understanding of Latex Allergies in the Health Care Worker according to the objectives listed. To earn contact hours from the American Society of PeriAnesthesia Nurses (ASPAN) Continuing Education Provider Program: (1) read the article; (2) complete the posttest by indicating the answers on the test grid provided; (3) tear out the page (or photocopy) and submit postmarked before February 28, 2005, with check payable to ASPAN (ASPAN member, $12.00 per test; nonmember, $15.00 per test); and (4) return to ASPAN, 10 Melrose Ave, Suite 110, Cherry Hill, NJ 08003-3696. Notification of contact hours awarded will be sent to you in 4 to 6 weeks.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
29
Posttest Questions 1. The increase in latex sensitivity has been triggered by the rise in all of the following diseases except . a. HIV b. TB c. hepatitis 2. On average, the first clinical symptoms of latex sensitivity occur exposure. a. 1 b. 2 c. 5 d. 10
year(s) after
3. The use of natural rubber approximates how many tons annually? a. 2,250,000 b. 4,500,000 c. 6,750,000 d. 9,000,000 4. Plant species that produce natural rubber include all of the following except a. dandelions b. sunflowers c. chrysanthemums d. azaleas
.
5. Rubber in its natural state is considered an allergen. a. True b. False 6. The adverse reaction that occurs when the immune system mistakenly identifies a similarly shaped protein molecule or chemical composition for an allergen is . a. true reactivity b. cross reactivity c. false reactivity d. mistaken reactivity 7. An IgE-mediated hypersensitivity involving antibodies on the mast cells and causing the mast cells to degranulate and release vasoactive and inflammatory mediators is . a. type I reaction b. type II reaction c. type III reaction d. type IV reaction 8. A delayed-type reaction mediated by helper T lymphocytes is a a. type I reaction b. type II reaction c. type III reaction d. type IV reaction
.
30
CAROLINE C. TESIOROWSKI
9. A type of contact dermatitis in which the skin above the glove line is spared from the skin reaction is . a. irritant contact b. allergic contact c. delayed contact d. immediate contact 10. Fruits that may cause a cross reaction with latex sensitivity include all of the following except . a. banana b. kiwi c. chestnut d. grapes
LATEX ALLERGIES IN THE HEALTH CARE WORKER ANSWERS System W010205/2. Please circle the correct answer 1. a. 2. a. b. b. c. c. d. 6. a. 7. a. b. b. c. c. d. d.
3.
8.
31
a. b. c. d. a. b. c. d.
4.
a. b. c. d. a. b. c. d.
9.
5.
a. b.
10.
a. b. c. d.
Please Print Name
Nursing License No/State
Address City
State
Zip
Social Security
ASPAN Member #
EVALUATION: Latex Allergies in the Health Care Worker (SD, strongly disagree; D, disagree; ?, uncertain; A, agree; SA, strongly agree)
1. To what degree did the content meet the objectives? a. Objective #1 was met. b. Objective #2 was met. c. Objective #3 was met. d. Objective #4 was met. 2. The program content was pertinent, comprehensive, and useful to me. 3. The program content was relevant to my nursing practice. 4. Self-study/home study was an appropriate format for the content. 5. Identify the amount of time required to read the article and take the test. 25 min 50 min 75 min 100 min 125 min Test answers must be submitted before February 28, 2005, to receive contact hours.
SD
D
?
A
SA
1 1 1 1 1 1 1 1 1
2 2 2 2 2 2 2 2 2
3 3 3 3 3 3 3 3 3
4 4 4 4 4 4 4 4 4
5 5 5 5 5 5 5 5 5
Latex Allergies in the Health Care Worker Caroline C. Tesiorowski, RN
A dramatic increase in the incidence of latex allergies in health care workers followed the surge in latex glove use accompanying the rise of human immunodeficiency virus (HIV) in the early 1980s. This increase in latex glove use was driven by the release of Universal Precautions issued by the Centers for Disease Control (CDC) in response to the rise of HIV and other blood-borne pathogens. Efforts to stem allergic responses in the workplace have relied on the substitution of other materials for latex. Unfortunately, there is so much latex in everyday life that avoiding this allergen is exceedingly difficult once one is sensitized. Additionally, there are numerous cross reactants that are present in the environment. The situation is further confounded by the introduction of genetically manipulated foods and agricultural products that contain defense proteins genetically inserted to protect plants from pests and pathogens. Many of these defense proteins are antigens that will cross react with latex. Sensitivity reactions, once developed, may progress to the point at which the health care worker is excluded from working. This report provides an overview of rubber products and cross reactants, allergic reactions, and latex sensitivity for the health care worker. © 2003 by American Society of PeriAnesthesia Nurses.
Objectives—Based on the content of this article, the reader should be able to (1) identify at least 3 plant species that produce natural rubber; (2) describe the relationship between the latex glove manufacturing process and latex sensitivity; (3) define the 4 types of allergic reactions; and (4) describe the diagnosis of latex allergy. SINCE 1987, THE number of workers’ compensation claims regarding latex sensitivity have increased significantly in the health care field. These claims involve workers in all health care
Caroline C. Tesiorowski, RN, is a nurse in the PACU at Santa Barbara Cottage Hospital, Santa Barbara, CA. Address correspondence to Caroline C. Tesiorowski, RN, 14 Calle Capistrano, Santa Barbara, CA 93105; e-mail address: [email protected]. © 2003 by American Society of PeriAnesthesia Nurses. 1089-9472/03/1801-0004$35.00/0 doi:10.1053/jpan.2003.50003 18
settings and specialties, including perianesthesia nurses.1 This increase in latex hypersensitivity was triggered by the advent of universal precautions after the rise in acquired immunodeficiency syndrome (AIDS), hepatitis C, and other blood-borne pathogens.2,3 This hypersensitivity, particularly in the health care worker, now raises an emergency public health issue. Margaret Veach, writing in the American Medical News, indicated that estimates of latex medical glove use had jumped from 12 billion pairs in 1987, to more than 200 billion pairs a decade Journal of PeriAnesthesia Nursing, Vol 18, No 1 (February), 2003: pp 18-31
LATEX ALLERGIES IN THE HEALTH CARE WORKER
later. Because the demand sometimes exceeded supply, some manufacturers were prone to cut corners on the processing necessary to remove allergens. Others, in their rush to the market, used less-expensive processes that actually increased these adverse characteristics.4
Significance of Latex Allergy in the Health Care Worker Latex allergies currently affect an estimated 10% to 12% of health care workers3,5 and up to 24% of anesthesiologists.5 It is estimated that 10% of these people are immunoglobulin E (IgE) positive and in the early stages of sensitization, but clinically asymptomatic.5 Others, however, estimate that the figure for those sensitized but not clinically having reactions may be as high as 50%.6 Based on the most conservative of these estimates, it is possible that an average of 2 to 5 PACU nurses of every 20 may already be sensitized.
19
erative setting, staff may still be continuously exposed in other areas of the hospital because airborne particulate matter remains an unresolved issue. The amount of particulate does not have to be extreme. Baur et al13 noted that the probable threshold for latex aeroallergens is 0.6 ng/m3 for health care workers who have been previously sensitized. Charous et al14 noted that even while using personal latex precautions, a dental assistant with latex allergy and occupational asthma was still exposed to latex aeroallergens in the workplace because of latex that had settled into or was part of clinic upholstery fabric, as well as carpet dust. Thus, merely controlling for latex in the particular workstation or job may be insufficient. Additionally, numerous and ubiquitous crossreacting allergens exist in most metropolitan and urban environments. Thus, even after removing oneself from the health care workplace, the highly sensitized individual may still be continuously exposed in an office situation in which this form of air pollution is a factor. For example, tire dust, an ubiquitous air pollutant in any metropolitan center, is an agonist allergen and cross reacts in natural rubber latex (NRL) allergy.15-19 It has also been found that birch pollen and certain other cereal-derived ␣-amylases exacerbate or cross react with rubber product materials.
Brown et al7 noted that latex sensitivity groups were twice as likely to be associated with an inherited or familial heightened sensitivity to allergens (atopy) as compared with nonsensitized groups. Atopy is characterized by a history of asthma, eczema, and allergic rhinitis. Studies show that on average, the first clinical symptoms appeared after 5 years of exposure in those using latex gloves in the workplace.8,9 This seems reasonable because about 6 years elapsed between the Centers for Disease Control’s (CDC) replacement of the “Blood and Body Fluids Precautions” with Universal Precautions in 1983, and the first major reports of latex reactions in 1989. Certain patient populations may offer a glimpse of the potential for developing hypersensitivity by repeated exposure. The theory of hypersensitivity by repeated exposure is further confirmed by the high percentage of reactivity (60% to 70%) found in children with spina bifida.10-12
The use of rubber in products is ubiquitous throughout society because the world’s natural rubber use currently approximates 4,500,000 tons annually.20 An understanding of rubber products and their cross reactants is crucial in the diagnosis and management of latex hypersensitivity.
Although some controls can be applied to limit exposure to latex allergens for sensitized patients and staff in the perianesthesia and periop-
Natural rubber latex is one of several products made from rubber. The term latex originally applied only to the sap of rubber-producing
Rubber Products and Cross Reactants
CAROLINE C. TESIOROWSKI
20
plants. With common use, however, the term has come to represent both the uncured natural and the synthetic rubber products. The term rubber is thought to come from an early serendipitous use in which a wad of the raw sap coagulant was found to rub off pencil marks in the British record books on rubber plantations. We now call this an eraser. The commercial applications of NRL include dipped goods such as gloves and condoms, as well as adhesives in pressure-sensitive tape. Approximately 40,000 household and medical products contain latex, making it difficult, if not impossible, to avoid contact with latex allergens.21-23 Although most natural rubber latex is obtained commercially from the Hevea braziliensis rubber tree, there are about 200 plant species that produce natural rubber. These include common dandelion, goldenrod, and members of the sunflower family. Sunflower has been shown to contain serious contact allergen contents. Nonetheless, there are several common members of this family that include many edible salad plants such as lettuce, endive, chicory, and artichoke. Other members of this family include chrysanthemums, as well as many common weeds and wildflowers. Also included are cultivated species such as marigolds, daisies, and sunflowers, the oils and seeds of which are found in many baked products.19 Unfortunately, species within the sunflower group will cross react with the plants within the Umbelliferae family, named for the umbrellashaped flowering stand.19 There are a surprisingly large number of plants in this family that are used as foods or spices. Examples include carrots, parsley, celery, and fennel. Additionally, there are discussions about nickel cross reacting with these plant materials.24 The principal protein molecule of rubber is 1-4 cis-polyisoprene (1-4 CP). This molecule, in common with natural rubber, is also found in many plant species. Data indicate that more
than 2,000 plant species contain 1-4 CP. This family of isoprenoids comprises more than 200,000 different molecules that are found in cell membranes and cellular structures of both plants and animals. Isoprenoids also act as electron carriers and are important in cellular energy. Numerous isoprenes are also involved in defense proteins built by plants against pests and pathogens.25,26 Rubber in its natural state generally is not considered an allergen.26 Nonetheless, in harvesting rubber, the trees are scribed to create wounds that drip sap. In response to this repeated wounding, the tree produces defense proteins that are incorporated into the sap that eventually becomes the latex product. Natural latex is comprised of somewhat more than 250 polypeptides, of which 60 have IgE-binding tendencies that may result in allergic reactivity.27 These polypeptides are chains of amino acids, and each protein is made up of one or more polypeptide chains. Several rubber proteins or their polypeptide fragments have been linked to allergies. Reaction to the 4.7-kDa polypeptide, Hevein, has been detected in enzyme-linked tests in 75% of the sera from health care workers allergic to latex. Positive skin test results to this polypeptide were also noted in 81% of patients with latex allergies.27-29 The 14-kDa rubber elongation factor (Hev b 1) is also a major player in the allergy.30 Other proteins identified as latex allergens include the following:
● ● ● ●
Hevein C domain, 14 kDa Prohevein, 20 kDa Profilin, 14 to 15 kDa Hevamin and other 29- to 33-kDa proteins ● 45-kDa protein ● 27-kDa in patients with spina bifida These proteins are absorbed in glove powder, which is an allergen carrier. In some gloves, these proteins leach out and become available to the skin.31,32
LATEX ALLERGIES IN THE HEALTH CARE WORKER
Rubber Processing Rubber processing is a vast complexity of chemical reactions. It requires the blending, at various critical stages, of a large host of chemical additives. These additives are used to give strength, elasticity, longevity, color, texture, and a myriad of other properties to rubber. Such chemicals also include flame retardants, fungicides, ultraviolet absorbers and blocking agents, stabilizers, and dozens of antioxidants to reduce deterioration.33-35 During the processing of sap from the rubber plant, ammonia is used to prevent coagulation and also to extend storage. Further processing, however, necessitates deammoniation, which requires formaldehyde. Formaldehyde was shown to sensitize up to 24% of patients in one study.33 In addition, there is also evidence of mutagenicity, as well as cases of lymphomas caused by formaldehyde.34,35 For these reasons, low ammonia sap processing is preferred. This technique, however, requires different chemicals for stabilization and preservatives. These chemicals may leach from the finished product, causing serious toxic effects. Chemicals associated with the more serious toxic effects are tetramethylthiram disulfide (examples of this chemical family include Antabuse and some commercial agricultural fungicides) and dithiocarbamate (related to the “nerve gas” cholinesterase-inhibiting pesticides). The thirams are in fact derivatives of dithiocarbamates. The combined alcohol-thiram (Antabuse) reaction is not an allergic response, but rather a toxic response accruing to enzyme blockage. When aldehyde dehydrogenase is blocked, this allows for the accumulation of toxic levels of acetaldehyde. Thus, topical exposure through latex gloves to thiram is sufficient to initiate an “Antabuse reaction” and can affect the innocent social drinker. The reaction can also exacerbate lesions of allergic contact dermatitis.26 Latex gloves are relatively easy to manufacture. Because of the high demand for cheap latex
21
gloves, many small and inexperienced foreign firms went into business during the initial peak demand of the mid to late 1980s. These firms attempted to produce high volumes with rushed production, leading to 2 significant results. The necessary wash and rinse cycle for the finished gloves was greatly reduced. More importantly, however, there was a tendency to overdose the latex with accelerators, activators, and sulfur to quicken the reaction time and machine speed. Unfortunately, this excessive use of additives and compounding ingredients exceeded the solubility in the rubber, allowing leaching, which then brought these additives as well as the reacting proteins into direct contact with the user and the patient. This extractable latex allergen level in latex gloves may vary more than 500-fold in different brands.36,37 These added chemicals can be highly toxic and are a main source of sensitizers. Additionally, rubber products may be admixtures of natural and synthetic rubbers. The distinction between rubber and plastic can also be spurious because both contain the same antioxidants, stabilizers, and catalysts.26 About one third of the chemicals used in rubber processing are also used in plastics.38 A classic example of the junction between rubber and plastic is polyurethane. This plastic is known to induce tissue reactions that produce very thick wound capsules around implanted devices.39
Cross Reactants When the immune system mistakenly identifies a similarly shaped protein molecule or chemical composition for an allergen, adverse reactions occur. This is known as cross reactivity. Such cross reactivity is caused by a wide number of structurally related proteins that plants can potentially produce, and that are mimicked in the cellular machinery of humans. Many of these defense proteins arise from ancient ancestral organisms that have common lineages with both plants and animals. Nature has thus produced highly conserved evolutionary processes for defense that worked for most of life’s evo-
CAROLINE C. TESIOROWSKI
22
lution and development, but now conflict with modern chemistry and genetically engineered foods and fibers.19 There are a wide number of natural and manmade environmental cross reactants that exacerbate latex sensitivity. Defense proteins are genetically engineered proteins for insertion into plant genes to improve their resistance to pests and diseases. More and more genetically modified foods are being produced that contain these defense proteins. Unfortunately, these products constitute major cross-reacting allergens with NRL. IgE-bound reactions occur with “prohevein,” which is one of the major allergens in NRL, and also to other proheveinlike defense proteins in 70% to 88% of persons allergic to NRL.40 Prohevein-like defense proteins are also found in tobacco.41 Thus, once sensitized to NRL, smokers and those exposed to “second-hand” smoke may see their health increasingly affected.
Allergic Reactions Allergic reactions are the most common form of immunologic response and involve the T and B cells in an antibody-immunoglobulin–mediated response to foreign antigens (allergens). The result can range from local tissue inflammation to systemic organ dysfunction. Of the 5 immunoglobulins present in the body, 3 are involved in allergic hypersensitivity reactions. These immunoglobulins are IgG, IgM, and IgE. The reactions stimulated by these immunoglobulins are classified into 4 distinct types (types I through IV). Type I Reaction
A type I reaction is an IgE-mediated hypersensitivity involving antibodies on the mast cells. Reaction with an allergen causes the mast cell to degranulate and release vasoactive and inflammatory mediators. The reaction occurs within minutes, and the result may be seen locally in such responses as allergic rhinitis, angioedema, or atopic dermatitis. Atopic individuals are more prone to experiencing this
reaction. Anaphylaxis is also a type I reaction. The antibody response in anaphylaxis is a generalized, whole-body response. Type II and III Reactions
Type II and III reactions involve both IgG and IgM. These types of reactions generally are not involved with latex. A type II reaction is seen in complement reactions associated with cellbound reactions and generally is not associated with allergens. Type III reactions are an immune complex hypersensitivity associated with an allergen that activates the complement cascade. With high concentrations of both allergen and antibody, an Arthus reaction may occur. This reaction generally results from an injection and is seen as a localized skin inflammation, at times with hemorrhage, and occasionally followed by necrosis and ulceration. In contrast to the more immediate type I reaction, a type III reaction develops over 4 to 10 hours.42-44 Type IV Reaction
Type IV reactions are delayed-type reactions mediated by helper T lymphocytes. These reactions are commonly seen in contact dermatitis with latent developing symptoms. Latex allergens may also be involved. Symptoms may begin to appear within 24 hours of exposure, but there can be a lag of several days. Poison oak would be an example of a type IV reaction. Another example of this reaction is the tuberculin reaction.44,45
Latex Reactions Latex reactions fall into either the type I (immediate type reaction) or type IV (delayed reaction) categories. Reactions noted may include vertigo, urticaria, contact dermatitis, naso-rhinitis, upper respiratory tract irritation, conjunctivitis, local angioedema, asthma, hypotension, and anaphylactic shock, which can end in death. Type I Allergic Reaction: The Immediate Reaction
Onset of symptoms for type I, the immediate reaction, may be seen as early as a few minutes
LATEX ALLERGIES IN THE HEALTH CARE WORKER
after exposure. For example, anaphylaxis in the operating theater usually starts within 30 minutes after the procedure is started. This rapid response is not necessarily the rule, however. A reaction involving complete collapse may also occur a few hours after exposure. Thus, the exposed nurse may finish the shift and be on a congested freeway when hit with anaphylaxis. Type I reactions to latex can include a wide range of signs and symptoms as shown in Table 1.44-46 Type IV Allergic Reaction: The Delayed Reaction
A type IV reaction is a delayed reaction that may occur hours after the exposure to the allergen. Type IV reactions often present as secondary lesions from contact dermatitis and arise from a loss of barrier function in the irritated skin and tissue. Dermatitis related to latex gloves is seen in 2 different forms; however, only one is an allergic response. The most common response is irritant contact dermatitis, which is a nonallergic response making up 75% of cases.43 Signs and symptoms are dry, itchy, irritated areas on the skin of the hands. Marked erythema is sharply demarcated, and this may be associated with numerous vesicles.42-44 Dermatitis distribution is the single most important clue in distinguishing the 2 reactions. With irritant contact dermatitis, the skin above the glove line is usually spared as the skin reaction arises from the irritation of the gloves and added powders.42,44 Allergic contact dermatitis is a type IV, T cell– mediated response comprising 25% of cases. Symptoms may appear in 24 hours and crest in about 48 hours. Each exposure builds greater sensitivity.43 This reaction results from the chemicals added to latex during harvesting, processing, or manufacturing. The pathophysiology requires a prior sensitizing contact to a specific allergen. There may be repeated contacts and no apparent reaction. The reaction to the allergen usually occurs at the site of contact anywhere from 5 to 7 days, and occasionally as long as 20 days after the initial or sensitizing
23
Table 1. Signs and Symptoms of Latex Allergy: Type I, the Immediate Reaction Atopic Allergic rhinitis, nasal and conjunctival discharge accompanied by pruritis, erythema, and excessive tearing Allergic asthma, hayfever, bronchial asthma accompanied by wheezing and tightness of the chest, dyspnea, and cough Allergic dermatitis, pruritis, hives accompanied by erythema with edema and pruritis, followed by vesicles and bullae. Later the skin weeps, followed by crusting and secondary infection Allergic gastroenteropathy from ingested allergens may be accompanied by skin reactions such as urticaria and angioedema. Anaphylactic Initial symptoms Tingling lips and mouth Flushing of face, body Itchy eyes, nose, face Eyes and face swelling Nausea Hives Wheezing Hoarseness Respiratory symptoms Dyspnea Retrosternal pain Stridor Tachypnea Wheezing Cardiovascular symptoms Palpitations Tachycardia Arrhythmias Hypotension Syncope Arrest Cutaneous symptoms Pruritis Edema Erythema Hives Gastrointestinal symptoms Nausea Vomiting Abdominal cramps Diarrhea Advancing symptoms of anaphylaxis Anxiety and feeling of doom Weakness and dizziness Laryngeal edema Laryngeal obstruction Inability to breath Shock Loss of consciousness Arrest Data from Calfran et al,44 Tierney et al,45 and AORN.46
24
contact. The site, once reacting, is characterized by a perivascular accumulation of mononuclear cells causing leaking of endothelial cells and microvascular permeability.44 There are no circulatory or otherwise detectable antibodies produced, although there is a local tissue allergy.43 On staining with immunoperoxidase, there is a predominance of CD4 T lymphocytes in the perivascular tissue. These lymphocytes then differentiate into T1 cells that secrete cytokines, the responsible mechanism for the delayed reaction.44 Symptoms may then develop in 24 to 48 hours after the second exposure to the allergen (6 hours to 7 days). The first symptoms, however, can develop after years of continued exposure. With removal of the offending allergen, the reaction will generally resolve after 2 to 3 weeks. Unfortunately, this condition is usually, though not invariably, lifelong. Thus, later recontact after a long period of isolation from the offending allergen may instigate the reappearance of the problem.42-44 Because rubber products are ubiquitous, there may be continued non-workplace exposures. In allergic eczematous contact dermatitis, the acute lesions may be red, swollen, and weeping. Crusting lesions may appear after a few days. In chronic cases, skin scaling and fissuring are dominant.42-44 In addition to latex gloves used at the work site, causes may include fabric finishes, dyes, oils, tars, rubber, soap, cosmetics and perfume, insecticides, wood resins, plants, paints, plastics, glues, fiberglass, metals, polishes, and ointments.43 This contact dermatitis may also be associated with medications. The main pharmacotherapeutic agents involved are rheumatologic agents, including NSAIDs. Dermatologic, ophthalmologic, pneumologic, and cardiovascular drugs are also implicated. These medications can include the caine anesthetics; antihistamines such as pyribenzamine; or antibiotics such as neomycin, furacin, penicillin, or sulfa. Because people often unconsciously rub their eyes, the eyelids also can be the site of intense edema and vesiculation with erythema.42-44 Type IV glove dermatitis can be reduced by switching to eudermic products. Health care
CAROLINE C. TESIOROWSKI
workers with type IV allergic responses can obtain the required level of job-related protection from nitrile, vinyl, or other synthetic gloves. When latex gloves are required, powder-free gloves with reduced protein content should be used. The term hypoallergenic does not necessarily mean that the gloves contain lower protein allergen content. Consequently, the designation as hypoallergenic should not be the main criterion in determining alternatives.47
Latex Allergy and the Health Care Worker Most forms of type I allergy caused by environmental allergens other than latex can be treated by pharmacotherapy or specific immunotherapy. The health care industry has adopted a policy of minimizing exposure to latex proteins through the provision of other materials. Originally, this was thought to represent a costeffective, preventative measure for latex allergy, especially in the hospital setting. Recent available studies, however, now seem to raise some questions as to whether simply replacing latex with nonallergenic materials is sufficient. Williams and Halsey48 showed the existence of extremely small respirable particulate matter associated with either the powder or a bacterial contaminate formed during the production of latex gloves. These small particles carry the latex allergen into the air and remain airborne for hours. Once airborne, these particles become part of the internal hospital air supply. The hospital’s large ventilation systems then assure that the particles are broadly distributed and recirculated.49 The last 2 decades have seen a rise in type I reactions from latex products. Initial reactions may start with relatively vague symptoms that include a suddenly stuffy nose, oropharyngeal swelling, and difficulty swallowing. This may be followed by anxiety, dyspnea, tachypnea, retrosternal pain and tightness of the chest, perspiration, and pallor. From there, full shock can develop. This reaction is now recognized as a rapidly growing clinical crisis.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
It is not merely the wearing of latex gloves that can affect the previously sensitized health care worker. The worker may be exposed in many ways that she/he would not suspect because these exposures are not limited to the work environment and may involve the health care worker as a patient. Tan et al50 and others51,52 discuss the perioperative collapse of patients who were previously sensitized to latex and cross reacted with certain anesthetic agents. Additionally, some cross sensitivity may occur with the use of alcohol to clean skin surfaces because alcohol and alcohol-containing lotions may react with thiram, a chemical used in the processing of latex. This reaction can lead to either continued skin sensitivity or an Antabuse reaction. Cross-reacting ingredients must also be considered in the planning and preparation of hospital meals because cases of anaphylactic reactions in hospital patients arising from cross reactivity with food items have been noted.53,54 Health care workers employed in large publicly funded health care systems may also be at increased risk as these and other systems often depend on the typical “least-cost” contractor for supplied items. Williams and Halsey48 showed that gram-negative bacterial endotoxins (GNBE) are a highly significant contaminant of some glove manufacturing processes. The effects of GNBE include skin irritation and the potential for accompanying secondary lesions, induced respiratory problems, fever, and shock. The highest levels of endotoxin were found in nonsterile examination gloves, an item that is often purchased on a “least-cost” contract. Although there was a greater tendency for powdered gloves to contain more endotoxins and reactive
25
proteins, this problem was also noted in nonpowdered gloves in which these highly respirable GNBE particles were mainly found on the inside of the gloves. These particles are not physically associated with the powder and are easily released into the air on the “explosive” snap as the gloves are pulled off. GNBE may be responsible for the disproportionate enhancement of delayed and immediate hypersensitivity reactions to the chemicals and proteins found in latex gloves. This problem may be exacerbated by sterilization, as Shmunes and Darby55 reported that sterilization of similar gloves by gamma irradiation actually increased the endotoxin levels. Further, it was found that the use of ethylene oxide caused a reaction with the rubber accelerators in gloves. The new products produced by this reaction were capable of causing irritant dermatitis and chemical burn. These effects did not dissipate with the gas but remained active for months in wrapped and stored materials.56-61 An initial development of hypersensivity to latex may affect not only one’s employment, but everyday activity as well. Numerous allergens of latex are also found to cross react with a broad variety of environmental allergens,62-64 thus raising the potential for hypersensitivity reactions outside of the work environment as well. Materials known to cross react with and exacerbate latex hypersensitivity are noted in Table 2.
Diagnosis of Latex Allergy Latex allergy should be ruled out for anyone developing the following symptoms after latex exposure: irritated red hands; irritation involving nasal passages, sinuses, eyes, shortness of
Table 2. A List of Common Latex Cross Reactants Fruits and nuts Apple, apricot, avocado, banana, cherry, chestnut, coconut, fig, kiwi fruit, loquat, mango, melons, papaya, passion fruit, peach, strawberries, sunflower seed, watermelon Vegetables Buckwheat, carrot, fresh yellow pepper, other peppers, potato, tomato, turnip Animal products Crustacea, fish, shellfish, snails Other allergens Auto tire dust, bacterial endotoxins, birch and cedar pollens, certain anesthetic agents, sunflower family, tobacco, Ficus benjamina
CAROLINE C. TESIOROWSKI
26
breath, coughing, or wheezing; hives; or unexplained shock. Health care workers experiencing these symptoms should be appropriately evaluated because once sensitized, continued exposure may end in a serious allergic reaction. Diagnosis entails a thorough medical history, physical examination, and laboratory tests. Food and Drug Administration (FDA)–approved blood tests are now available for detecting latex antibodies. Additionally, there are standardized protocols for skin tests; however, no standardized latex extract is currently available. Skin testing extracts to determine latex protein allergy include commercial extracts, latex glove extracts, and extracts of hevea leaves. Testing has to be performed with the allergen against which the patient is presumed to be allergic. The different types of available allergen extracts, however, may not contain the particular allergen. One extract used in Canada (Bencard Laboratories, Mississauga, Ontario) has been reported to have 93% sensitivity to latex.65 Glove extracts are made using a standardized method of soaking glove material in diluent. Extreme caution must be used with glove extracts because of variable allergenic protein levels and the potential for serious reactions from skin tests.66,67 Conversely, false-negative skin tests may also be produced by extracts of gloves with low latex allergen content. Skin testing with allergen extracts has traditionally been considered the most sensitive means of detecting IgE antibodies. Although often considered the gold standard, this process is not without risk and therefore should be performed only at medical centers with staff that are experienced and equipped to handle severe reactions. The pinprick introduces latex into the skin and a positive result produces dermal edema and reddening. Certain fruits such as banana, avocado, chestnut, and kiwi fruit (Table 2) may cross react with latex in allergy testing in the atopic individual. If the health care worker is also exposed to glutaraldehyde (Cidex, Sporocidin), testing for this should also be included.
Allergens that should be routinely tested include the following68: black rubber mix, 1%; carba mix, 3%; ethylenediamine 2HCL, 1%; imidazolodinyl urea, 2%; mercaptobenzothiazole, 1%; mercapto mix, 1%; O-phenylenediamine, 1%; thiram mix, 1%; triclosan, 2%; volunteersupplied latex glove. In vitro tests are available and are safer because the laboratory can determine the presence of IgE antibodies specific to latex from a drawn blood sample. A number of tests exist in the marketplace that give good results with freedom from the danger of immediate hypersensitivity associated with skin-prick testing.69 For the interested reader, more information may be found on the American Society of Anesthesiology Web page, www.asahq.org/Newsletters/ 1999/05_99/Latex_0599.html.70 Once sensitized to latex, individuals may need to considerably alter their current lifestyle to accommodate the ubiquitous nature of latex and cross reactants. At some point, the hypersensitivity may reach a level at which there is a considerable risk for the development of anaphylactic shock. The individual would then need to carry self-injecting equipment for continued safety. With the added insults to the immune system, there is the added risk of multiple chemical sensitivity syndrome.71-73 This syndrome is controversial but is recognized in worker compensation claims, tort liability, and regulatory actions. Unfortunately, once this level of disability is achieved, little can be done for the lost earning power, and current government support and compensation programs offer a dismal prospect.
Conclusion Latex sensitivities in health care workers continue to rise. Reactions are often dramatic and unpredictable because a mild sensitivity can convert to anaphylactic shock after multiple or continued exposure. An awareness of reaction classifications, exposure routes, and diagnosis techniques is critical in avoiding continued exposure and possible adverse outcomes.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
27
References 1. Gelman JL: United States Workers’ Compensation Programs are Becoming Sensitized to Latex. Update on the Law. . . Latex Allergy Litigation. Volume 21, Issue 7. November 1999. Available at www.gelmans.com/articles/latexsurvey99/ latexsurvey1199l.htm. Accessed December 23, 2002 2. Chardin H, Desvaux FX, Mayer C, et al: Protein and allergen analysis of latex mattresses. Int Arch Allergy Immunol 119:239-246, 1999 3. Mahler V, Fischer S, Fuchs T, et al: Prevention of latex allergy by selection of low-allergen gloves. Clin Exp Allergy 30:509-520, 2000 4. Veach M: Allergies to latex gloves hand health workers a growing concern. Available at www.latexallergylinks.tripod. com. Accessed June 14, 2002 5. Holzman RS, Katz JD: Editorial reviews. Anesthesiology 89:287-289, 1998 6. Kowalczyk L: Allergy hazard: Growing number of health care workers developing dangerous reactions to latex. Patriot Ledger April 1, 1997, pp 1-2 7. Brown RH, Schauble JF, Hamilton RG: Prevelance of latex allergy among anesthesiologists. Anesthesiology 89:292-299, 1998 8. Allmers H, Kirchner B, Huber H, et al: The latency period between exposure and symptoms in allergy to natural latex. Deutche Med Wochen 121:823, 1996 9. Esterhuizen TM, Hnizdo E, Rees D: Occurrence and causes of occupational asthma in South Africa—Results from SORDSA’s Occupational Asthma Registry, 1997-1999. S Afr Med J 91:509-513, 2001 10. Elsworth PL, Merguerian PA, Klein RB, et al: Evaluation and risk factors of latex allergy in spina bifida patients: Is it preventable? J Urol 150:691-693, 2001 11. Konz KR, Gjia JK, Kurup VP, et al: Comparison of latex hypersensivity among patients with urologic defects. J Allergy Clin Immunol 95:950-954, 1995 12. Kattan H, Harfi HA, Tipirneni P: Latex allergy in Saudi children with spina bifida. Allergy 54:70-73, 1999 13. Baur X, Chen Z, Allmers H: Can a threshold limit value for natural rubber latex airborne allergens be defined? J Allergy Clin Immunol 101:24-27, 1998 14. Charous BL, Schuenemann PJ, Swanson MC: Passive dispersion of latex aeroallergen in a health care facility. Ann Allergy Asthma Immunol 85:285-290, 2000 15. Williams PB, Buhr MP, Weber RW, et al: Latex allergen in respirable particulate air pollution. J Allergy Clin Immunol 95:88-95, 1995 16. Williams PB, Akasawa A, Dreskin S, et al: Respirable tire fragments contain specific IgE-binding and bridging latex antigens. Chest 109:13S, 1996 (suppl 3) 17. Pope CA, Thun MJ, Namboodiri MM, et al: Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. Am J Respir Crit Care Med 151:669-674, 1995 18. Miguel AG, Cass GR, Weiss J, et al: Latex allergens in tire dust and airborne particles. Environ Health Perspct 104:11801186, 1996 19. Vallon C, Sainte-Laudy J, Guerin JC: Asthma by proxy (to latex of a condom). General review based on an observation. Allerg Immunol (Paris) 26:248-256, 1994 20. GillenA:Biopolymers—Naturalrubber.Availableatwww. Naturalrubber.cjb.net. Accesses June 14, 2002
21. Redman MC: Latex allergy: Recognition and perioperative management. J Post Anesth Nurse 11:6-9, 1996 22. Goffin V, Kharfi M, Pierard-Franchimont C, et al: Latex allergy—When uncertainty remains the only certainty. Rev Med Liege 56:165-169, 2001 23. Latex allergy alert—Update. Available at www.specialclothes.com/latex.htm. Accessed June 17, 2002 24. Ricciardi L, Gangemi S, Isola S, et al: Nickel allergy, a model of food cellular hypersensitivity? Allergy 56:109-112, 2001 (suppl 67) 25. D’Auzac J: From sucrose to rubber: Hevea as a “green rubber factory.” Physiology of latex production. Available at www.irrdb.org/hevea/auzac. Accessed December 16, 2002 26. Taylor JS: Rubber, in Fisher AA (ed): Fisher’s Contact Dermatitis (ed 3). Philadelphia, PA, Lea & Febiger, 1986 27. Posch A, Chen-Heimsoth M: Latex allergens: A review of current knowledge. Pneumologie 51:1058-1062, 1977 28. Kurup VP, Yeang HY, Sussman GL, et al: Detection of immunoglobulin antibodies in the sera of patients using purified latex allergens. Clin Exp Allergy 30:359-369, 2000 29. Chen Z, Posch A, Lohaus C, et al: Isolation and identification of hevin as a major IgE-binding polypeptide in Hevea latex. J Allergy Clin Immunol 99:402-409, 1997 30. Rauf-Heimsoth M, Chen Z, Rihs HP: Analysis of T-cell reactive regions and HLA-DR4 binding motifs on latex allergen Hev b 1 (rubber elongation factor). Clin Exp Allergy 28:339348, 1998 31. Tomazic VJ, Shampaine EL, Lamanna A, et al: Cornstarch powder on latex products is an allergen carrier. J Allergy Clin Immunol 93:751-758, 1994 32. Lundberg M, Wrangsjo K, Johansson SGO: Latex allergens in glove powdering slurries. Allergy 50:378-380, 1995 33. Epstein E, Maibach HI: Formaldehyde allergy. Arch Dermatol 94:186, 1966 34. Speit G, Merk O: Evaluation of mutagenic effects of formaldehyde in vitro: Detection of crosslinks and mutations in mouse lymphoma cells. Mutagenesis. 17:183-187, 2002 35. Merk O, Speit G: Significance of formaldehyde-induced DNA-protein crosslinks for mutagenesis. Environ Mol Mutagen 32:260-268, 1998 36. Jones R, Scheppmann D, Heilman D, et al: Prospective study of extractable latex allergen contents of disposable medical gloves. Ann Allergy 73:321-325, 1994 37. Yunginger J, Jones R, Fransway A, et al: Extractable latex allergens and proteins in disposable medical gloves and other rubber products. J Allergy Clin Immunol 93:836-842, 1994 38. Blue Book. Materials, compounding ingredients and machinery for rubber. New York, NY, Bill Publishing, 1983 39. Shanklin DR, Smalley DL: Dynamics of wound healing after silicon device implantation. Exp Mol Pathol 67:26-39, 1999 40. Bowles DJ: Defense-related proteins in higher plants. Ann Rev Biochem 59:873-907, 1990 41. Hanninen AR, Kalkkinen N, Mikkola JH, et al: Proheveinlike defense proteins of tobacco is a cross reactive allergen for latex-allergic patients. J Allergy Clin Immunol 106:778-779, 2000 42. Odom WD, James RB, Berger TG (eds): Andrews’ Diseases of the Skin: Clinical Dermatology (ed 9), Philadelphia, PA, Saunders, 2000 43. Sheard C: Contact dermatitis. Internet Dermatology So-
CAROLINE C. TESIOROWSKI
28
ciety, Stamford, Connecticut. Last update February 2, 1997. Available at www.lemedicine.org/contact.htm. Accessed June 17, 2002 44. Coltran RS, Kumar V, Collins T (eds): Robbins Pathologic Basis of Disease (ed 6). London, England, Saunders, 1999, pp 195-206 45. Tierney LM, McPhee SJ, Papadakis MA (eds): CMDT (ed 3). Norwalk, CT, Appelton & Lang, 1994, pp 655-657 46. AORN: AORN latex guideline from Standards, Recommended Practices and Guidelines 1999. Denver, CO, Assn of Operating Room Nurses Inc, 1999, p 107 47. A Hazard Alert From the Department of Labor and Industries About Latex Allergy. November 1997. Available at www.lni.wa.gov/wisha/hazalerts/hz972.htm. Accessed December 16, 2002 48. Williams PB, Halsey JF: Endotoxin as a factor in adverse reactions to latex gloves. Ann Allergy Asthma Immunol 79:303310, 1997 49. Charous BL, Schuenemann PJ, Swanson MC: Passive dispersion of latex aeroallergen in a health care facility. Ann Allergy Asthma Immunol 85:285-290, 2000 50. Tan BB, Lear JT, Watts J, et al: Perioperative collapse: Prevalence of latex allergy in patients sensitive to anesthetic agents. Contact Dermatitis 36:47-50, 1977 51. Laxenaire MC, Mertes PM: Anaphylaxis during anaesthesia. Results of a two-year survey in France. Br J Anaesth 87:549-558, 2001 52. Baulig W, Fisy B, Otto G, et al: Latex allergy. Perioperative management in anesthesia and cardiac anesthesia. Anaesthesist 50:861-868, 2001 53. Abeck D, Boerries M, Kuwert C, et al: Anaphylactic reactions to food items with latex allergy. Hautarzt 45:364-367, 1994 54. Ganglberger E, Radauer C, Wagner S, et al: Hev b 8, the Hevea brasiliensis latex profilin, is a cross-reactive allergen of latex, plant foods and pollen. Int Arch Allergy Immunol 125: 216-227, 2001 55. Shmunes E, Darby T: Contact dermatitis due to endotoxin in irradiated latex gloves. Contact Derm 10:240, 1984 56. Taylor JS: Dermatologic hazards from ethylene oxide. Cutis 19:198, 1977 57. Sexton RJ, Henderson EV: Dermatological injuries by ethylene oxide. J Ind Hyg Tox 31:29, 1949 58. Leonard JC, Morin C: Industrial progress concerning
latex allergy in surgery. Rev Chir Orthop Reparatrice Appar Mot 85:727-730, 1999 59. Romaguera C, Vilaplana J: Airborne occupational contact dermatitis from ethylene oxide. Contact Derm 39:85, 1998 60. Tiukhtin VG: Gas chromatographic determination of ethylene oxide residue in sterilized medical items. Gig Sanit Jan-Feb(1) :50-51, 1996 61. Baranova NI, Rudenko BA, Likhtman TV: Gas chromatographic determination of micro-quantities of ethylene oxide in polymeric articles for medical use. Gig Sanit Apr(4) :64-66, 1985 62. Hanninen AR, Mikkola JH, Kalkkinen N, et al: Increased allergen production in turnip (Brassica rapa) by treatments activating defense mechanisms. J Allergy Clin Immunol 104: 194-201, 1999 63. Blanco C, Carillo T, Castillo R, et al: Latex allergy: Clinical features and cross-reactivity with fruits. Annl Allergy 73:309-314, 1994 64. Blanco Guerra C: Latex-fruit syndrome. Allergol Immunopathol (Madr) 30:156-163, 2002 65. Turjanmaa K, Reunala T, Alenius H, et al: Allergens in latex surgical gloves and glove powder. Lancet 336:1588, 1990 66. Yunginger JW: Diagnostic skin testing for natural rubber latex allergy. J Allergy Clin Immunol 102:351-352, 1998 67. Yunginger JW: Latex allergy in the workplace: An overview of where we are. Ann Allergy Asthma Immunol 83:630633, 1999 68. Vyas A, Pickering CA, Oldham LA, et al: Survey of symptoms, respiratory function, and immunology and their relation to glutaraldehyde and other occupational exposures among endoscopy nursing staff. Occup Environ Med 57:752759, 2000 69. Preventing Allergic Reactions to Natural Rubber Latex in the Workplace. Washington, DC, NIOSH, June 1997, DHHS (NIOSH) Publication No. 97-135 70. Thomas LC, Skerman JH: Latex allergy: Another complication for anesthesiology, part 2. Available at www.asahq.org/ Newsletters/1999/05_99/Latex_0599.html. Accessed December 16, 2002 71. Gots RE: Multiple chemical sensitivities—Public policy. [Editorial] J Toxicol Clin Toxicol 33:111-113, 1995 72. American Medical Association Council on Scientific Affairs: Clinical ecology. JAMA 268:3465-3467, 1992 73. Miller CS: Chemical sensitivity: Symptom, syndrome or mechanism for disease? Toxicology 111:69-86, 1996
Latex Allergies in the Health Care Worker 1.2 Contact Hours Directions: The multiple choice examination below is designed to test your understanding of Latex Allergies in the Health Care Worker according to the objectives listed. To earn contact hours from the American Society of PeriAnesthesia Nurses (ASPAN) Continuing Education Provider Program: (1) read the article; (2) complete the posttest by indicating the answers on the test grid provided; (3) tear out the page (or photocopy) and submit postmarked before February 28, 2005, with check payable to ASPAN (ASPAN member, $12.00 per test; nonmember, $15.00 per test); and (4) return to ASPAN, 10 Melrose Ave, Suite 110, Cherry Hill, NJ 08003-3696. Notification of contact hours awarded will be sent to you in 4 to 6 weeks.
LATEX ALLERGIES IN THE HEALTH CARE WORKER
29
Posttest Questions 1. The increase in latex sensitivity has been triggered by the rise in all of the following diseases except . a. HIV b. TB c. hepatitis 2. On average, the first clinical symptoms of latex sensitivity occur exposure. a. 1 b. 2 c. 5 d. 10
year(s) after
3. The use of natural rubber approximates how many tons annually? a. 2,250,000 b. 4,500,000 c. 6,750,000 d. 9,000,000 4. Plant species that produce natural rubber include all of the following except a. dandelions b. sunflowers c. chrysanthemums d. azaleas
.
5. Rubber in its natural state is considered an allergen. a. True b. False 6. The adverse reaction that occurs when the immune system mistakenly identifies a similarly shaped protein molecule or chemical composition for an allergen is . a. true reactivity b. cross reactivity c. false reactivity d. mistaken reactivity 7. An IgE-mediated hypersensitivity involving antibodies on the mast cells and causing the mast cells to degranulate and release vasoactive and inflammatory mediators is . a. type I reaction b. type II reaction c. type III reaction d. type IV reaction 8. A delayed-type reaction mediated by helper T lymphocytes is a a. type I reaction b. type II reaction c. type III reaction d. type IV reaction
.
30
CAROLINE C. TESIOROWSKI
9. A type of contact dermatitis in which the skin above the glove line is spared from the skin reaction is . a. irritant contact b. allergic contact c. delayed contact d. immediate contact 10. Fruits that may cause a cross reaction with latex sensitivity include all of the following except . a. banana b. kiwi c. chestnut d. grapes
LATEX ALLERGIES IN THE HEALTH CARE WORKER ANSWERS System W010205/2. Please circle the correct answer 1. a. 2. a. b. b. c. c. d. 6. a. 7. a. b. b. c. c. d. d.
3.
8.
31
a. b. c. d. a. b. c. d.
4.
a. b. c. d. a. b. c. d.
9.
5.
a. b.
10.
a. b. c. d.
Please Print Name
Nursing License No/State
Address City
State
Zip
Social Security
ASPAN Member #
EVALUATION: Latex Allergies in the Health Care Worker (SD, strongly disagree; D, disagree; ?, uncertain; A, agree; SA, strongly agree)
1. To what degree did the content meet the objectives? a. Objective #1 was met. b. Objective #2 was met. c. Objective #3 was met. d. Objective #4 was met. 2. The program content was pertinent, comprehensive, and useful to me. 3. The program content was relevant to my nursing practice. 4. Self-study/home study was an appropriate format for the content. 5. Identify the amount of time required to read the article and take the test. 25 min 50 min 75 min 100 min 125 min Test answers must be submitted before February 28, 2005, to receive contact hours.
SD
D
?
A
SA
1 1 1 1 1 1 1 1 1
2 2 2 2 2 2 2 2 2
3 3 3 3 3 3 3 3 3
4 4 4 4 4 4 4 4 4
5 5 5 5 5 5 5 5 5